Fear conditioning ptsd,mass gain diet plan pdf,learn to say no - Plans On 2016

Post-traumatic Stress Disorder (PTSD) encompasses intrusive traumatic memories, which dictate behavior. Using typical Pavlovian fear conditioning and extinction paradigms, the researchers first investigated the disparity between recent and remote memories.
To investigate what made the remote memories more robust, post-mortem chemical analyses were carried out.
These results led the researchers to test whether increasing the likelihood of acetylation would affect the outcome of extinction training.
Inevitably, however, as this was a preclinical trial using mice, this research has several shortcomings.
Nonetheless, this is a promising avenue of research, which not only offers the possibility of better treatments for PTSD, but advances our understanding of how memories are represented in the brain. This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
PTSD is a pathological condition that may affect war veterans, emergency personnel and other individuals that become highly anxious and confused when encountering conditions that remind them of stressful situations, although the actual danger no longer exists. Overall, this is an excellent example of translational research performed in animals that has great potential to improve human health. About Todd French I have 20 years of research and teaching experience, with a Master's in Cell Biology and a Ph.D.
Extinction is a form of learning in which a conditional stimulus (CS) is presented alone after conditioning.
Department of Psychiatry, University of Illinois at Chicago and Mental Health Service Line, Jesse Brown VA Medical Center, Chicago, Illinois 60608, USA. VA Ann Arbor Healthcare System and Departments of Psychology, Psychiatry and Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109, USA. Stephen MarenStephen Maren is Professor of Psychology and a member of the Institute for Neuroscience at Texas A&M University in College Station, Texas, USA.
JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser. Describe how Pavlov’s early work in classical conditioning influenced the understanding of learning. Review the concepts of classical conditioning, including unconditioned stimulus (US), conditioned stimulus (CS), unconditioned response (UR), and conditioned response (CR). Explain the roles that extinction, generalization, and discrimination play in conditioned learning. In the early part of the 20th century, Russian physiologist Ivan Pavlov (1849–1936) was studying the digestive system of dogs when he noticed an interesting behavioral phenomenon: The dogs began to salivate when the lab technicians who normally fed them entered the room, even though the dogs had not yet received any food. Pavlov had identified a fundamental associative learning process called classical conditioning. As you can see in Figure 12.7 "4-Panel Image of Whistle and Dog", psychologists use specific terms to identify the stimuli and the responses in classical conditioning. Top left: Before conditioning, the unconditioned stimulus (US) naturally produces the unconditioned response (UR).
Conditioning is evolutionarily beneficial because it allows organisms to develop expectations that help them prepare for both good and bad events.
After he had demonstrated that learning could occur through association, Pavlov moved on to study the variables that influenced the strength and the persistence of conditioning.
Although at the end of the first extinction period the CS was no longer producing salivation, the effects of conditioning had not entirely disappeared.
Pavlov also experimented with presenting new stimuli that were similar, but not identical to, the original conditioned stimulus. The flip side of generalization is discriminationThe tendency to respond differently to stimuli that are similar, but not identical.—the tendency to respond differently to stimuli that are similar but not identical. In some cases, an existing conditioned stimulus can serve as an unconditioned stimulus for a pairing with a new conditioned stimulus—a process known as second-order conditioningConditioning that occurs when an existing conditioned stimulus serves as an unconditioned stimulus for a new conditioned stimulus.. As we have seen in Chapter 16 "Introducing Psychology", scientists associated with the behavioralist school argued that all learning is driven by experience, and that nature plays no role.
Clinical psychologists make use of classical conditioning to explain the learning of a phobiaA strong and irrational fear of a specific object, activity, or situation.—a strong and irrational fear of a specific object, activity, or situation.
Classical conditioning has also been used to help explain the experience of posttraumatic stress disorder (PTSD), as in the case of P.
Posttraumatic stress disorder (PTSD) represents a case of classical conditioning to a severe trauma that does not easily become extinct. PTSD develops because the emotions experienced during the event have produced neural activity in the amygdala and created strong conditioned learning.
In classical conditioning, a person or animal learns to associate a neutral stimulus (the conditioned stimulus, or CS) with a stimulus (the unconditioned stimulus, or US) that naturally produces a behavior (the unconditioned response, or UR). Extinction occurs when the CS is repeatedly presented without the US, and the CR eventually disappears, although it may reappear later in a process known as spontaneous recovery. Stimulus generalization occurs when a stimulus that is similar to an already-conditioned stimulus begins to produce the same response as the original stimulus does. Stimulus discrimination occurs when the organism learns to differentiate between the CS and other similar stimuli. In second-order conditioning, a neutral stimulus becomes a CS after being paired with a previously established CS. Some stimuli—response pairs, such as those between smell and food—are more easily conditioned than others because they have been particularly important in our evolutionary past. Recall a time in your life, perhaps when you were a child, when your behaviors were influenced by classical conditioning. If posttraumatic stress disorder (PTSD) is a type of classical conditioning, how might psychologists use the principles of classical conditioning to treat the disorder?
Science, Technology and Medicine open access publisher.Publish, read and share novel research. Cellular Mechanisms in the Amygdala Involved in Memory of Fear ConditioningRyong-Moon Shin[1] National Institute of Radiological Sciences, Japan1. SR-8993 is a non addictive synthetic compound that performs similarly in mice, and has the potential to treat humans suffering from PTSD safely and effectively.
Kerry Ressler is a professor at Emory University’s Yerkes National Primate Research Center in Atlanta, GA.  His laboratory is focused on the molecular and cellular mechanisms of fear learning, utilizing the power of molecular genetics to understand the molecular biology, neural circuitry, and the behavioral biology of fear. Such CS-alone presentations decrease the magnitude and frequency of the learned response, and this loss of responding to the CS is context-specific.
His research seeks to understand the brain circuits and cellular mechanisms underlying the encoding, retrieval and extinction of aversive memories, and how dysfunction in these circuits and processes contributes to anxiety disorders. Therefore, the study of fear and its inhibition are essential in understanding the disorder. Pavlov realized that the dogs were salivating because they knew that they were about to be fed; the dogs had begun to associate the arrival of the technicians with the food that soon followed their appearance in the room. He conducted a series of experiments in which, over a number of trials, dogs were exposed to a sound immediately before receiving food.
The unconditioned stimulus (US)Something (such as food) that naturally triggers a response.
Top right: Before conditioning, the neutral stimulus (the whistle) does not produce the salivation response. Imagine, for instance, that an animal first smells a new food, eats it, and then gets sick.
In some studies, after the conditioning had taken place, Pavlov presented the sound repeatedly but without presenting the food afterward.
Pavlov found that, after a pause, sounding the tone again elicited salivation, although to a lesser extent than before extinction took place. If conditioning is again attempted, the animal will learn the new associations much faster than it did the first time. For instance, if the dog had been conditioned to being scratched before the food arrived, the stimulus would be changed to being rubbed rather than scratched. Pavlov’s dogs quickly learned, for example, to salivate when they heard the specific tone that had preceded food, but not upon hearing similar tones that had never been associated with food.
In one of Pavlov’s studies, for instance, he first conditioned the dogs to salivate to a sound, and then repeatedly paired a new CS, a black square, with the sound. Classical conditioning, which is based on learning through experience, represents an example of the importance of the environment. For example, driving a car is a neutral event that would not normally elicit a fear response in most people. Although people may in some cases develop a driving phobia, they are more likely to develop phobias toward objects (such as snakes, spiders, heights, and open spaces) that have been dangerous to people in the past. In this case the original fear response, experienced during combat, has become conditioned to a loud noise. As a result of this association, the previously neutral stimulus comes to elicit the same response (the conditioned response, or CR). Eventually, the students start becoming quiet and attentive whenever the teacher approaches the chalkboard. Describe in detail the nature of the unconditioned and conditioned stimuli and the response, using the appropriate psychological terms. Membrane physiological characters of two representative cells of the LA.Typical firing patterns of the two neurons recorded under current-clamp mode in response to increasing current injection steps. Feedfoward GABA receptor-mediated inhibition of principal neuron is stronger in thalamic input.
Maren, 2001Is There Savings for Pavlovian Fear Conditioning after Neurotoxic Basolateral Amygdala Lesions in Rats?
SR-8993 is being further evaluated for its potential use in treating human stress-related disorders such as PTSD. This chapter will provide detailed protocols for fear conditioning and extinction which can be used as a model to further understand and study PTSD.
Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder.
He systematically controlled the onset of the sound and the timing of the delivery of the food, and recorded the amount of the dogs’ salivation.
Bottom left: The unconditioned stimulus (US), in this case the food, is repeatedly presented immediately after the neutral stimulus. If the animal can learn to associate the smell (CS) with the food (US), then it will quickly learn that the food creates the negative outcome, and not eat it the next time. Spontaneous recovery: After a pause, when the CS is again presented alone, the behavior may again occur and then again show extinction. The increase in responding to the CS following a pause after extinction is known as spontaneous recoveryThe increase in responding to the conditioned stimulus (CS) after a pause that follows extinction.. He found that the dogs also salivated upon experiencing the similar stimulus, a process known as generalization.
Discrimination is also useful—if we do try the purple berries, and if they do not make us sick, we will be able to make the distinction in the future.
Eventually he found that the dogs would salivate at the sight of the black square alone, even though it had never been directly associated with the food. But if a person were to experience a panic attack in which he suddenly experienced strong negative emotions while driving, he may learn to associate driving with the panic response. In modern life, it is rare for humans to be bitten by spiders or snakes, to fall from trees or buildings, or to be attacked by a predator in an open area. When the person with PTSD hears a loud noise, she experiences a fear response even though she is now far from the site of the original trauma. The graphs represent electrophysiological recordings of the LTP observed in cortical (A) and thalamic (B) inputs in the presence of PTX and without PTX.
LTP in thalamic input to the LA was induced by the presynaptic stimulation without postsynaptic depolarization (A).
Now Japan suffers triple disasters: massive earthquake, vast tsunami and the world`s worst nuclear crisis.
Davis, (1995, Involvement of subcortical and cortical afferents to the lateral nucleus of the amygdala in fear conditioning measured with fear- potentiated startle in rats trained concurrently with auditory and visual conditioned stimuli. Sacchtti, Role of secondary sensory cortices in emotional memory storage and retrieval in rats.
Epigenetic Priming of Memory Updating during Reconsolidation to Attenuate Remote Fear Memories, Cell, 156 (1-2) 261-276. They also found that an abnormal variant of Oprl1 gene in humans is associated with a history of childhood trauma and PTSD.
Ressler is a Howard Hughes Medical Institute Investigator and a practicing psychiatrist, with an interest in translational and clinical research of fear-based psychiatric disorders. The figure shows the typical procedure for studying the context-dependence of extinction in rodents.
Initially the dogs salivated only when they saw or smelled the food, but after several pairings of the sound and the food, the dogs began to salivate as soon as they heard the sound. After the association is learned, the previously neutral stimulus is sufficient to produce the behavior.
Bottom right: After learning, the neutral stimulus (now known as the conditioned stimulus or CS), is sufficient to produce the conditioned responses (CR).
As you can see, after the intial acquisition (learning) phase in which the conditioning occurred, when the CS was then presented alone, the behavior rapidly decreased—the dogs salivated less and less to the sound, and eventually the sound did not elicit salivation at all. When Pavlov again presented the CS alone, the behavior again showed extinction until it disappeared again.


GeneralizationThe tendency to respond to stimuli that resemble the original conditioned stimulus. And we can learn that although the two people in our class, Courtney and Sarah, may look a lot alike, they are nevertheless different people with different personalities.
Secondary conditioners in everyday life include our attractions to things that stand for or remind us of something else, such as when we feel good on a Friday because it has become associated with the paycheck that we receive on that day, which itself is a conditioned stimulus for the pleasures that the paycheck buys us.
Nature also plays a part, as our evolutionary history has made us better able to learn some associations than others. PTSD is a severe anxiety disorder that can develop after exposure to a fearful event, such as the threat of death (American Psychiatric Association, 1994).American Psychiatric Association. The same protocol did not induce LTP in cortical input (B).The course of LTP in thalamic input experiment by using unitary EPSAC recording (C). The victims with fear in their minds deeply might fall into fear-related disorders in future. Collins, 2000Neuronal Correlates of Fear in the Lateral Amygdala: Multiple Extracellular Recordings in Conscious Cats. Luan Phan is Professor of Psychiatry at the University of Illinois at Chicago, USA, and Associate Head of Clinical and Translational Research and Chief of Neuropsychiatric Research at the Jesse Brown VA Medical Center (Chicago, Illinois).
The conditioned stimulus (CS)A neutral stimulus that, after being repeatedly presented prior to the unconditioned stimulus, begins to evoke a similar response as the unconditioned stimulus. ExtinctionThe reduction in responding that occurs when the conditioned stimulus is presented repeatedly without the unconditioned stimulus. Fear is a conserved emotion in response to danger and triggers some defensive mechanisms for adapting to threatening events for survival. Le Doux, 1990Synaptic plasticity in fear conditioning circuits: induction of LTP in the lateral nucleus of the amygdala by stimulation of the medial geniculate body. Le Doux, 1999Why we think plasticity underlying Pavlovian fear conditioning occurs in the basolateral amygdala. Bucy, 1937Psychic blindness` and other symptoms following bilateral temporal lobectomy in rhesus monkeys.
Shinnick-Gallagher, 1997Fear conditioning induces a lasting potentiation of synaptic currents in vitro. Le Doux, 1997Organization of intraanygdaloid circuitries in the rat: an emerging framework for understanding function of the amygdala. Le Doux, 1992Equipotentiality of thalamo-amygdala and thalamo-cortico-amygdala circuits in auditory fear conditioning.
Subsequently, extinction training to that CS occurs in another context (either the purple or green context), and rats are then tested in a context that is either the same or different as the one in which extinction took place. His current work takes an affective cognitive neuroscience approach to elucidate neuromarkers of recovery and resilience and treatment mechanisms in anxiety and mood disorders. In his experiment, high school students first had a brief interaction with a female experimenter who had short hair and glasses. Luthi, 2003Presynaptic induction of heterosynaptic associative plasticity in the mammalian brain. Luthi, 2008Fear conditioning and long-term potentiation in the amygdale: what really is the connection? Moore, 2001Role of NMDA, non-NMDA, and GABA receptors in signal propagation in the amygdala formation. In this example, the purple context is the same context as extinction for half of the animals but a different context for the other half of the animals.
In Pavlov’s experiment, the sound of the tone served as the conditioned stimulus that, after learning, produced the conditioned response (CR)An acquired response to the formerly neutral stimulus., which is the acquired response to the formerly neutral stimulus. If we eat some red berries and they make us sick, it would be a good idea to think twice before we eat some purple berries. The study was set up so that the students had to ask the experimenter a question, and (according to random assignment) the experimenter responded either in a negative way or a neutral way toward the students. Defining the cellular and synaptic mechanisms underlying fear memory will enhance our understanding of biological mechanism to enemies, as well as our ability to develop treatments for individual afflicted with anxiety disorders, including posttraumatic stress disorder (PTSD).The discovery of long-term potentiation (LTP), a phenomenon in which repetitive stimulation of afferent fibers results in a prolonged enhancement of synaptic strength provided the cellular mechanism to explain learning and memory formation. Romanski, 1990The lateral amygdaloid nucleus: sensory interface of the amygdala in fear conditioning. Le Doux, 1997Fear Conditioning Enhances Different Temporal Components of Tone-Evoked Spike Trains in Auditory Cortex and Lateral Amygdala. Bolshakov, 2006Spatiotemporal asymmetry of associative synaptic plasticity in fear conditioning pathways. Bolshakov, 2004Glutamate uptake determines pathway specificity of long-term potentiation in the neural circuitry of fear conditioning.
Bolshakov, 2007Norepinephrine enables the induction of associative long-term potentiation at thalamo-amygdala synapses.
Le Doux, 2000The amygdala modulates memory consolidation of fear-motivated inhibitory avoidance learning but not classical fear conditioning.
He is an American College of Neuropsychopharmacology Fellow and Past President of the Psychiatric Research Society. Note that the UR and the CR are the same behavior—in this case salivation—but they are given different names because they are produced by different stimuli (the US and the CS, respectively).
Although the berries are not exactly the same, they nevertheless are similar and may have the same negative properties. Then the students were told to go into a second room in which two experimenters were present, and to approach either one of them. While LTP has been described at many synapses in different brain regions, it has been studied most intensively at glutamatergic synapses in the mammalian hippocampus. Davis, 1990Blocking of acquisition but not expression of conditioned fear-potentiated startle by NMDA antagonists in the amygdale. Le Doux, 2001Intra-amygdala blockade of the NR2B subunit of the NMDA receptor disrupts the acquisition but not the expression of fear conditioning. Le Doux, 1999aL-type voltage-gated calcium channels mediate NMDA-independent associative long-term potentiation at thalamic input synapses to the amygdala. His research focus is on the neurobiology and the neuroanatomy of stress, negative emotions and cognitive–emotional interactions in patients with post-traumatic stress disorder and in healthy individuals.
However, the researchers arranged it so that one of the two experimenters looked a lot like the original experimenter, while the other one did not (she had longer hair and no glasses). However, linking changes in synapse transmission of the hippocampus to specific behavioral changes has proved to be difficult largely because of the complex behaviors which the hippocampus is involved in.We have to apply a simpler system to investigate such changes. Luthi, 2005Dendrite spine heterogeneity determines afferent-specific Hebbian plasticity in the amygdala. Morozov, 2009Selective gating of glutamatergic inputs to excitatory neurons of amygdala by presynaptic GABAb receptor. The students were significantly more likely to avoid the experimenter who looked like the earlier experimenter when that experimenter had been negative to them than when she had treated them more neutrally. Auditory fear conditioning induces LTP-like enhancement of synaptic transmission in cortical input to the principal neurons of the amygdala that both mimic and occlude LTP in acute slice induced with electrical stimulation, thus providing a simple linkage between changes of synaptic strength and behavior in auditory fear conditioning (Tsvetkov et al., 2002). Morozov, (2008, Enhanced cortico-amygdala efficary and suppressed fear in absence of Rap 1. Bolshakov, 2002Fear conditioning occludes LTP-induced presynaptic enhancement of synaptic transmission in the cortical pathway to the lateral amygdale.
The participants showed stimulus generalization such that the new, similar-looking experimenter created the same negative response in the participants as had the experimenter in the prior session. The conservation of the anatomy and physiology of the amygdala between species allows studies in different animals to get potential implications for fear memory and associated disorders in human.
Malinow, 2007Emotion Enhances Learning via Norepinephrine Regulation of AMPA-Receptor Trafficking. Bolshakov, 2006Synaptically released zinc gates long-term potentiation in fear conditioning pathways. Le Doux, 2001Two different lateral amygdala cell populations contribute to the initation and storage of memory. Bolshakov, 2010Hierarchical order of coexisting pre- and postsynaptic forms of long-term potentiation at synapses in amygdale. In short, people with PTSD have developed very strong associations with the events surrounding the trauma and are also slow to show extinction to the conditioned stimulus. Garcia discovered that taste conditioning was extremely powerful—the rat learned to avoid the taste associated with illness, even if the illness occurred several hours later. We will focus on the lateral nucleus of amygdala (LA) because molecular and synaptic changes in this area have been shown to make essential contributions to the fear memory formation, storage, and expression of the learned fear (LeDoux, 1998).
Luthi, 2011A disinhibitory microcircuit for associative fear learning in the auditory cortex. But conditioning the behavioral response of nausea to a sight or a sound was much more difficult.
To get a better understanding synaptic mechanism underlying the learned fear, we firstly will review auditory fear conditioning in detail and the basic anatomy and properties of synaptic transmission of the LA. Bolshakov, 2012Coactivation of thalamic and cortical pathways induces input timing-dependent plasticity in amygdala. A meta-analysis of D-cycloserine and the facilitation of fear extinction and exposure therapy.
These results contradicted the idea that conditioning occurs entirely as a result of environmental events, such that it would occur equally for any kind of unconditioned stimulus that followed any kind of conditioned stimulus. Secondly we will summarize the molecular mechanisms that contribute to synaptic plasticity in the auditory fear conditioning. Bolshakov, 2002Identification of signaling network in lateral nucleus of amygdala important for inhibiting memory specifically related to learned gear. Rather, Garcia’s research showed that genetics matters—organisms are evolutionarily prepared to learn some associations more easily than others. Although neutral and aversive information enters via both thalamic and cortical inputs to the LA, the individual role of both inputs are still debated.
You can see that the ability to associate smells with illness is an important survival mechanism, allowing the organism to quickly learn to avoid foods that are poisonous.
Luthi, 2007A pathway- specific function for different AMPA receptor subunits in amygdala long-term potentiation and fear conditioning.
Rosen, 1996Response and Habituation of the Humanamygdala during visual processing of facial expression. The involvement of the amygdala in the learned fearThe most detailed behavioral studies from bilateral lesion of the primate temporal lobe suggest that the temporal lobe including amygadala is involved in processing emotion(Kluver & Bucy, 1937).
Bolshakov, 2005stathmin, a gene enriched in the amygdale, controls both learned fear and innate fear. Cognitive enhancers as adjuncts to psychotherapy: use of D-cycloserine in phobic individuals to facilitate extinction of fear. In this study, monkeys with bilateral temporal lobe lesions tried to eat inedible objects, to copulate with same-sex partners or even with other species, and lost their fear of snakes. The key feature of this phenomenon, called psychic blindness by Kluver and Bucy(1937), was seemed to lose their emotional implications despite their fine visual perception. In experiment using functional magnetic resonance imaging, human amygdalae was preferentially activated by emotional stimuli such as fearful faces (Breiter et al. These reports suggested that the amygdala plays an important role on processing emotion in response to aversive stimulus.
In rodent experiment, anatomical tracing and lesion studies indicated the importance of the LA for encoding fear memory. Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future. In particular, bilateral infusion of N-methyl-D-aspartate (NMDA) receptor antagonist, D-2-amino-5-phosphonovaleric acid (D-AP5) into the rat LA decreased the amount of the learned fear (Miserendino et al., 1990). This result suggests two possibilities: the first is that we can confirm that the amygdala is the very important region which fear memory could be stored. The second is that NMDA receptor-dependent plasticity change can occur in the amygdala during fear memory formation. Effects of beta blockade, PTSD diagnosis, and explicit threat on the extinction and retention of an aversively conditioned response. Moreover, fear conditioning induced LTP-like enhancement of synaptic transmission in auditory input to the LA the occlude NMDA receptor-dependent LTP in acute slice induced by electrical stimulation (Tsvetkov et al., 2002).
Changes in heart rate during conditioned suppression in rats as a function of US intensity and type of CS. Auditory fear conditioning provides an animal model that is commonly used to study associative learning, such as fear conditioning. Heart rate and general activity alterations of dogs during several aversive conditioning procedures.
During conditioning, neutral stimulus to experimental animal is paired with an aversive stimulus. Following a single or a few such pairing, the neutral stimulus elicits a defensive response as if he is threatened by an aversive stimulus. As subsequent presentation of the CS without the US elicits, in the conditioned animal,defensive behavioral responses (freezing responses), autonomic nervous system responses (change in blood pressure and heart rate) and neuroendocrine responses (release of hormones from the pituitary and adrenal glands). Some of these defensive responses are genetically determined: animals are innate species-specific responses to threats and express defensive responses automatically despite appropriate stimuli.
In fear conditioning, therefore, when the CS is used as an initially biological insignificant stimulus, such as sound, light or touch, experimental animals can show learned “fear” that had never occurred in response to the neutral CS. In the laboratory, the experimental cage for fear conditioning, equipped with stainless-steel shocking grids and a sound making apparatus, is placed in a sound-attenuating enclosure.


Pharmacological and anatomical analysis of fear conditioning using the fear-potentiated startle paradigm. For unpaired control group (Figure 1E), animal receives tones and footshocks in an unpaired manner (tones and footshock are separated by random intervals of some minutes). During the test 24-72 hours after training, animals areplaced in a novel cage in which the tone that had been presented during trainingis given after habituation period. However, animals also exhibits fear response in the absence of CS when returned to the chamber in which the tone and footshock were paired or unpaired. During fear conditioning (B), the electric footshock (US) is paired with an auditory sound several times. The sound is presented alone in the test session to estimate the effects of conditioning (C). To assess the amount of learned fear, most researcher measure the time of “freezing” behavior elicited by the auditory sound alone. During fear conditioning, an auditory sound is co-terminated with a footshock (D: paired group).
An unpaired group in which the auditory sound and electric footshock in a nonoverlapping manner (E). Here, this section will summarize the neuronal network about the flow of CS (auditory sound) and US (electric footshock).
Anatomical tracing studies combined with single unit recording in experimental animals suggest that the LA is a site of convergence of somatosensory input carrying the information relative to the footshock US and afferent inputs carrying the CS information (whatever the sensory modality) (Pitkanen et al., 1997).
Therefore, it has been suggested that the LA is the site, where the association of learned information about CS and US apparently occurs during fear conditioning (Fanselow & LeDoux, 1999). During auditory fear conditioning, the sensory information that mediates the CS (an audible cue), reaches the LA by the two pathways, both of which are essential to the learned fear (Romanski & LeDoux, 1992). The second input, the indirect cortico-amygdala projections, extends from the ventral division of the thalamic medial geniclulate nucleus (MGv) to the auditory cortex (TE) and includes further projections that relay the auditory information from the cortex to the LA (Maren, 2001).
Acquisition of contextual Pavlovian fear conditioning is blocked by application of an NMDA receptor antagonist D,L-2-amino-5-phosphonovaleric acid to the basolateral amygdala. Because auditory-evoked responses recorded in the different parts of the amygdala were the shortest in the LAd, it has been suggested that this part of the amygdala constitutes the entrance site to the fear conditioning (Bordi &LeDoux, 1992). After the information is processed in the LA, the final signals are sent to periaqueductal gary and brain stem via the central nucleu of the amygdala (CE), resulting in freezing, autonomic responses and release of stress hormones as the index of fear expression. Memory consolidation of auditory pavlovian fear conditioning requires protein synthesis and protein kinase A in the amygdala.
Convergence of CS and US enter in the LA, especially in the LAd, leading to synaptic plasticity.
Finally CE promotes some defensive responses, freezing, increased blood pressure and heart rate as the expression of conditioned fearby trigger of hypothalamic and brainstem areas. Stress-induced activation of prefrontal cortex dopamine turnover: blockade by lesions of the amygdala. The electrophysiological properties of the LAWe are just beginning to explore the properties of basic synaptic physiology in the LA for synaptic mechanism underling fear conditioning because the LA is the site where the CS and the US information convey and encoding fear memory is formed (LeDoux et al., 1990).
LeDoux et al (1990) has reported that bilateral lesion of the LA impaired fear conditioning.It is necessary to characterize the properties of neuron typing, excitatory and inhibitory synapse and neural network involving distinct types of neurons.
I will describe the rules governing and modulation of synaptic plasticity in the next subchapter 6. The whole-cell patch-clamp technique has widely been used to explore the synaptic character in the amygdala because the LA is not highly laminar, making field potential observations difficult. Training-induced changes in the expression of GABAA-associated genes in the amygdala after the acquisition and extinction of Pavlovian fear. By fine investigation of in vitro two-photon microscopy, the size of dendritic spines contacted by thalamic, with the ability large Ca2+transients during action potential backpropagation, was larger than that by cortical input to the principal cell of the LA. This thalamic spine could induce Hebbian plasticity by activation of R-type voltage-dependent Ca2+channel in input–specific manner (Humeau et al., 2005).
Consolidation of extinction learning involves transfer from NMDA-independent to NMDA-dependent memory.
The afferent projections from thalamic nucleus or auditory cortex to the LA form excitatory synapses on both principal neurons and inhibitory interneurons (Rainnie et al., 1991a, b). The studies by using intracellular recording from rat acute slice indicated that postsynaptic potentials elicited stimulation of the LA is composed of excitatory postsynaptic potentials (EPSPs) followed by either a fast inhibitory postsynaptic potential (f-IPSP) only, or by a fast- and subsequent slow-IPSP (s-IPSP).
L-type voltage-gated calcium channels are required for extinction, but not for acquisition or expression, of conditional fear in mice. The f-EPSPs increased in amplitude with membrane hyperpolarization and was insensitive to the NMDA receptor antagonist, D-AP5, butwas blocked non-NMDA receptor antagonist, 6-cyano-7-nitro-quinoxaline-2, 3-dione (CNQX). Like extinction, latent inhibition of conditioned fear in mice is blocked by systemic inhibition of L-type voltage-gated calcium channels. Moreover, fine electrophysiological studies indicated that the glutamatergic inputfrom both cortical and thalamic to principal cell of the LA do not differ in either theirbasal probability or quantal amplitude (Shin et al., 2006). Plus, both inputs do not overlap (Tsvetkov et al., 2004), indicating that both cortical and thalamic input to the LA are independent from each other. It has been reported that the vesicular Zn2+released from cortical, but not thalamic afferents, to the principal cell of the LA can induce NMDA receptor-dependent LTP (Kodirov et al., 2006). NMDA receptor are also functionally expressed at both cortico- and thalamo- LA synapses becomes evident at membrane depolarization. Pharmacological studies using the selective NR2A antagonist ifenprodil and the NR2A antagonist NVP-AAM077 have indicated that subunit composition of synaptic NMDA receptors in cortical input is not different from that in thalamic pathway (Shin et al., 2006). Regulation of gephyrin and GABAA receptor binding within the amygdala after fear acquisition and extinction. The cannabinoid receptor agonist WIN 55,212-2 facilitates the extinction of contextual fear memory and spatial memory in rats.
Inhibitory transmissionAs described above, Rainnie et al (1991a) showed that the EPSPs recorded in the LA are, followed by both fast- and slow-IPSPs.
Both IPSPs were reduced the presence of APV, and were abolished by CNQX, indicating that both IPSPs were mediated by multi-synapse pathways.
The CNQX-resistant fast-IPSPs were abolished by bicuculline methiodide, GABAA receptor antagonist, suggesting direct inhibition by local GABAegic circuit.
Inhibition of fatty-acid amide hydrolase accelerates acquisition and extinction rates in aspatial memory task. The slow-IPSP, which reversal potential is deeper (-95 mV), was depressed by 2-hydroxy-saclofen, GABAB receptor antagonist (Rainnie et al., 1991b). The inhibitory interneurons send inhibitory inputs to principal neurons and other interneurons and their feedback and feed-forward GABAergic inputs to principal neurons determine how the information conveying to principal neurons are processed (Wang et al., 2001). Figure 4.Feedfoward GABA receptor-mediated inhibition of principal neuron is stronger in thalamic input.
Regulation of extinction-related plasticity by opioid receptors in the ventrolateral periaqueductal gray matter. A leftward shift in the input-output curves obtained in thalamic input, as compared with those in cortical pathway was observed (Figure 4B). These results indicate the stronger inhibitory drive in thalamic pathway, as compared to cortical input.
Synaptic mechanism for fear memoryThe hypothesis that NMDA-dependent LTP is involved in the cellular mechanism underlying fear conditioning arose initially from the finding that blockade of NMDA receptor within the LA decreased the amount of learned fear (Miserendino et al., 1990). These synaptic modifications, observed along behavioural responses of learned fear, are mechanically similar to LTP induced artificially by electrical stimulation in acute slices of the LA. The NMDA receptor-dependent LTP induced by a pairing protocol (low-frequency presynaptic stimulation with postsynaptic depolarization) in the cortico-amygdala pathway was occluded in the acute slice of the conditioned rat (Tsvetkov et al., 2002). This result indicated that the NMDA receptors in the cortico-amygdala synapse are critical for fear conditioning. LTP induced by pairing protocol in the both the cortico- and thalmo-amygdala synapses required NMDA receptor activation (Shin et al., 2006). In addition, injection of NR2B subunit antagonist into the LA reduced the acquisition of fear conditioning without affecting expression of fear memories or basal synaptic transmission (Rodrigues et al., 2001). Hyperarousal does not depend on trauma-related contextual memory in an animal model of Posttraumatic Stress Disorder. In vivo electrophysiological recording of principal cells in the LA display unusually low firing pattern even during emotional arousal (Pare & Collins, 2000), providing that local GABAergic interneuron circuit`s tight inhibitory control on the excitabilityof principal neurons in the LA.
Therefore, it is thought that LTP in the LA is significantly diminished when pairing protocol is delivered in the absence of GABAA receptor antagonist.
A mouse model of posttraumatic stress disorder that distinguishes between conditioned and sensitised fear. Moreover, Hu et al (2007) have reported that emotion can enhance memory via norepinephrine regulation AMPA receptortrafficking into glutamatergic synapse. In addition, the highly expressed gastrin-releasin peptide in the LA suppressed both the fear conditioning responses and the magnitude of LTP recorded in cortical input.
Stress-induced enhancement of fear learning: an ­animal model of posttraumatic stress disorder.
Although the persistent increased synaptic strength in both thalamic and cortical inputs to the LA contributed to fear conditioning, the specific roles of both inputs are still debated. Lasting anxiogenic effects of feline predator stress in mice: sex differences in vulnerability to stress and predicting severity of anxiogenic response from the stress experience.
In vivo study revealed that the increasedpotential of the LA by stimulation of the auditory thalamus was observed, indicating that projections from the auditory thalamus to the LA are critical for auditory fear conditioning (Clugnet & LeDoux, 1990). In addition, rapid plasticity change occurred in the auditory thalamus rather than the auditory cortex during fear conditioning (Quirk et al., 1997).
A pilot randomized controlled trial of combined trauma-focused CBT and sertraline for childhood PTSD symptoms. Also,post-training lesion of cortical, but not thalamic input to the LA, abolished the learned fear, indicating that cortical input may be a dominant role in fear conditioning in intact brain (Campeau & Davis, 1997).
A pilot study of modified cognitive-behavioral therapy for childhood traumatic grief (CBT-CTG). It has been reported that presynaptic GABAB receptor in the LA prevented the generalization of the learned fear via the regulation of LTP in cortical, but not thalamic input to the LA, by using genetic deletion technique (Shaban et al., 2006).
Further, presynaptic GABAB receptor was also reported to suppress LTP in cortical input to the principal cell of the LA via the control of glutamate release in acute slice experiment (Pan et al., 2009). Post-traumatic stress disorder and other co-morbidities in a sample population of patients with irritable bowel syndrome. ConclusionBasic synaptic mechanisms in the amygdala that support auditory fear processes are now commonly known.
First: between the thalamic and cortical inputs, which is the afferent that control auditory fear conditioning? Second: Is it the pre- or postsynaptic modification of the induction and expression of LTP that is important during fear conditioning? Sex differences, context preexposure, and the immediate shock deficit in Pavlovian context conditioning with mice. A proposed test battery and constellations of specific behavioral paradigms to investigate the behavioral phenotypes of transgenic and knockout mice. Behavioral profiles of inbred strains on novel olfactory, spatial and emotional tests for reference memory in mice.
Genetic and behavioral differences among five inbred mouse strains commonly used in the production of transgenic and knockout mice.
Behavioral phenotypes of inbred mouse strains: implications and recommendations for molecular studies. Overtraining does not mitigate contextual fear conditioning deficits produced by neurotoxic lesions of the basolateral amygdala. Different Training Procedures Recruit Either One or Two Critical Periods for Contextual Memory Consolidation, Each of Which Requires Protein Synthesis and PKA Learn Mem.
A role for brain glucocorticoid receptors in contextual fear conditioning: dependence upon training intensity.
Fear conditioning and shock intensity: the choice between minimizing the stress induced and reducing the number of animals used.
Dorsal hippocampus involvement in delay fear conditioning depends upon the strength of the tone-footshock association. Administration of corticosterone after memory reactivation disrupts subsequent retrieval of a contextual conditioned fear memory: dependence upon training intensity. Protein synthesis is required for the enhancement of long-term potentiation and long-term memory by spaced training.
The inverted “u-shaped” dose-effect relationships in learning and memory: modulation of arousal and consolidation. Automated assessment of pavlovian conditioned freezing and shock reactivity in mice using the video freeze system. Evaluation of an improved automated analysis of freezing behaviour in rats and its use in trace fear conditioning.
Olfactory-mediated fear conditioning in mice: simultaneous measurements of fear-potentiated startle and freezing.




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